Abstract

Background

People living with HIV have higher sudden cardiac death (SCD) rates compared with the general population. Whether HIV infection is an independent SCD risk factor is unclear.

Methods and Results

This study evaluated participants from the Veterans Aging Cohort Study, an observational, longitudinal cohort of veterans with and without HIV infection matched 1:2 on age, sex, race/ethnicity, and clinical site. Baseline for this study was a participant's first clinical visit on or after April 1, 2003. Participants were followed through December 31, 2014. Using Cox proportional hazards regression, we assessed whether HIV infection, CD4 cell counts, and/or HIV viral load were associated with World Health Organization (WHO)–defined SCD risk. Among 144 336 participants (30% people living with HIV), the mean (SD) baseline age was 50.0 years (10.6 years), 97% were men, and 47% were of Black race. During follow‐up (median, 9.0 years), 3035 SCDs occurred. HIV infection was associated with increased SCD risk (hazard ratio [HR], 1.14; 95% CI, 1.04–1.25), adjusting for possible confounders. In analyses with time‐varying CD4 and HIV viral load, people living with HIV with CD4 counts < 200 cells/mm3 (HR, 1.57; 95% CI, 1.28–1.92) or viral load > 500 copies/mL (HR, 1.70; 95% CI, 1.46–1.98) had increased SCD risk versus veterans without HIV. In contrast, people living with HIV who had CD4 cell counts > 500 cells/mm3 (HR, 1.03; 95% CI, 0.90–1.18) or HIV viral load < 500 copies/mL (HR, 0.97; 95% CI, 0.87–1.09) were not at increased SCD risk.

Conclusions

HIV infection is associated with increased risk of WHO‐defined SCD among those with elevated HIV viral load or low CD4 cell counts.

Document Type

Article

Publication Date

9-8-2021

Notes/Citation Information

Published in Journal of the American Heart Association.

Copyright © 2021 The Authors

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

Digital Object Identifier (DOI)

https://doi.org/10.1161/JAHA.121.021268

Funding Information

This work was supported by National Institutes of Health grant HL126555 (Drs Tseng and Freiberg). VACS acknowledges the support of contracts AA020794, AA020790, AA020795, AA020799, and AA013566 from the National Institute on Alcohol Abuse and Alcoholism for this research.

Related Content

Supplementary Material for this article is available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.121.021268. It is also available for download as the additional file listed at the end of this record.

jah36632-sup-0001-datas1-tables1.pdf (95 kB)
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